Increases in glomerular cellularity and accumulation of extracellular matrix material are prominent histologic findings in a number of clinical and experimental glomerular diseases. Transforming growth factor-beta (TGF-beta) has been identified as a potentially important modulator of glomerular pathology based on its demonstrated ability to regulate proliferation and extracellular matrix synthesis by cultured glomerular cells. In addition, we have previously demonstrated that normal rat glomeruli contain high concentrations of TGF-beta1 and TGF-beta2 and that glomeruli possess unique TGF-beta binding proteins or receptors. The goal of these studies is to better understand the actions and mechanisms of action of TGF-beta in the glomerulus. The current focus of these studies is on TGF-beta binding proteins and receptors. We have identified subpopulations of type I and II receptors which have different affinities for TGF-beta1 and TGF-beta2. Evaluation of TGF-beta receptors in CHO cells demonstrated that: (1) all of the type I receptors and the majority of type II receptors have a density (determined with sucrose density gradients) which much greater than that predicted by their molecular weight, and (2) the subpopulations of type I and II TGF-beta receptors with differing affinities for TGF-beta1 and TGF-beta2 can be separated by sucrose gradient centrifugation. These findings are consistent with the hypothesis that differences in affinities of type I and II TGF-beta receptors for TGF-beta1 and TGF- beta2 are due to their participation in different types of receptor complexes.